Cervical spondylotic myelopathy is a common entity. It is clear that it is associated with both neural compression and motion. A tremendous amount of research is ongoing to investigate the cellular mechanisms responsible for the neurological deficits. Treatment consists of decompression and fusion.—Vincent Traynelis, MD

A review article by Etheridge and Kalantar in the June Seminars in Spine Surgery presents an update on the pathophysiology and biologic mechanisms of cervical spondylotic myelopathy—a common degenerative disease that results from spinal cord compression.The molecular pathology of cervical spondylotic myelopathy is believed to be related to ischemia and apoptosis.Static and Dynamic Mechanisms
Compression of the spinal cord may result from static mechanisms, such as degeneration of the intervertebral discs with aging, formation of osteophytes that narrow the cervical spinal canal, ectopic bone formation near the spinal canal (eg, ossification of the posterior longitudinal ligament and ligamentum flavum), and a genetic predisposition to have a tightened spinal canal. The compression also may result from dynamic mechanisms, which primarily involve excess motion of the spine due to traumatic injuries.

Biologic Mechanisms
The molecular pathology of cervical spondylotic myelopathy is believed to be related to ischemia and apoptosis. When the spinal cord is compressed, decreased blood flow to the spinal cord may occur, leading to ischemia and initiating an apoptotic cascade. This cascade is believed to most severely impact oligodendrocytes and causes demyelination of neurons in the spinal cord. This nerve damage and resultant debilitating symptoms may remain even after surgical decompression.

The mechanisms behind the myelopathic symptoms associated with this condition are unclear.

Treatment ofCervical Spondylotic Myelopathy
Surgical decompression of the spine is used to improve neurologic symptoms of this condition. The surgical approach may be anterior or posterior, and commonly involves fusion of multiple spinal levels to minimize movement of the spine after decompression. Significant relief of symptoms may result from surgical decompression; however, many patients continue to experience ongoing neurologic deficits after surgery resulting from the trauma caused by spinal compression.

No options are currently available to treat the damage caused on a molecular level. The authors call for future research to better understand the sequence of molecular events that occur following spinal cord damage to develop effective treatments.